Background Epidemiological studies have shown that both active and passive cigarette smoking increase the risk of atherosclerosis. But very little is known about the biological processes induced by passive cigarette s...Background Epidemiological studies have shown that both active and passive cigarette smoking increase the risk of atherosclerosis. But very little is known about the biological processes induced by passive cigarette smoking that contribute to atherosclerosis. We observe the expression of a few of biological and inflammatory markers in human arterial walls in vitro which were treated with the second-hand smoke solution （sidestream whole, SSW）, and discuss the possible mechanism of inflammatory injury induced by second-hand smoke. Methods The biological markers （platelet endothelial cell adhesion molecule-I, PECAM-1; a-smooth muscle actin, a-SMA; collagen IV, Col IV） and inflammatory markers （vascular cell adhesion molecule-1, VCAM-1; monocyte chemoattractant protein-1, MCP-1 ; interleukin-8, IL-8） of human aortat wall were tested by immunofluorescence staining. The levels of MCP-1 and IL-8 mRNA expression were detected by reverse transcription-polymerase chain reaction （RT-PCR）. Results No distinct difference was observed between SSW and the control group on the expression of biological markers as assessed by the light microscope. But the inflammatory markers VCAM-1, MCP-1 and IL-8 on the subendothelial layer and smooth muscle cell layers, which are near the endothelium of arterial wall, were strongly stained in the SSW group compared with the control group. Their fluorescence intensities in the 1：40 SSW group （VCAM-1： 0.35±0.04, MCP-1： 0.34±0.05, IL-8： 0.37±0.05） and the 1：20 SSW group （VCAM-I： 0.40±0.04, MCP-1： 0.52±0.09, IL-8： 0.51±0.07） were significantly stronger than the control group （VCAM-1： 0.12±0.04, MCP-1： 0.06±0.02, IL-8： 0.24±0.03） by semi-quantitative analysis of immunofluorescence （P 〈0.001 vs control）. MCP-1 mRNA expression in the 1：40 SSW （0.15±0.04） and the 1：20 SSW （0.19±0.06） group was significantly higher than in the control group （0.09±0.03） （P 〈0.05, P 〈0.01 vs control）; IL-8 mRNA expression in the 1：40 SSW （0.64±0.12） and 1：20 SSW （0.72±0.13） groups was also significantly higher than that in the control group （0.49±0.13） （P 〈0.05, P 〈0.01 vs control） by RT-PCR. Conclusions It is implied that a second-hand smoke solution induces the inflammatory reaction of the arterial wall by release of inflammatory factors even though there is no distinct structural change on the arterial walls under light microscope, indicating that passive cigarette smoking is related to inflammatory injury in human arterial wall and could be closely related to the early inflammatory stage of atherosclerosis.展开更多
文摘Background Epidemiological studies have shown that both active and passive cigarette smoking increase the risk of atherosclerosis. But very little is known about the biological processes induced by passive cigarette smoking that contribute to atherosclerosis. We observe the expression of a few of biological and inflammatory markers in human arterial walls in vitro which were treated with the second-hand smoke solution （sidestream whole, SSW）, and discuss the possible mechanism of inflammatory injury induced by second-hand smoke. Methods The biological markers （platelet endothelial cell adhesion molecule-I, PECAM-1; a-smooth muscle actin, a-SMA; collagen IV, Col IV） and inflammatory markers （vascular cell adhesion molecule-1, VCAM-1; monocyte chemoattractant protein-1, MCP-1 ; interleukin-8, IL-8） of human aortat wall were tested by immunofluorescence staining. The levels of MCP-1 and IL-8 mRNA expression were detected by reverse transcription-polymerase chain reaction （RT-PCR）. Results No distinct difference was observed between SSW and the control group on the expression of biological markers as assessed by the light microscope. But the inflammatory markers VCAM-1, MCP-1 and IL-8 on the subendothelial layer and smooth muscle cell layers, which are near the endothelium of arterial wall, were strongly stained in the SSW group compared with the control group. Their fluorescence intensities in the 1：40 SSW group （VCAM-1： 0.35±0.04, MCP-1： 0.34±0.05, IL-8： 0.37±0.05） and the 1：20 SSW group （VCAM-I： 0.40±0.04, MCP-1： 0.52±0.09, IL-8： 0.51±0.07） were significantly stronger than the control group （VCAM-1： 0.12±0.04, MCP-1： 0.06±0.02, IL-8： 0.24±0.03） by semi-quantitative analysis of immunofluorescence （P 〈0.001 vs control）. MCP-1 mRNA expression in the 1：40 SSW （0.15±0.04） and the 1：20 SSW （0.19±0.06） group was significantly higher than in the control group （0.09±0.03） （P 〈0.05, P 〈0.01 vs control）; IL-8 mRNA expression in the 1：40 SSW （0.64±0.12） and 1：20 SSW （0.72±0.13） groups was also significantly higher than that in the control group （0.49±0.13） （P 〈0.05, P 〈0.01 vs control） by RT-PCR. Conclusions It is implied that a second-hand smoke solution induces the inflammatory reaction of the arterial wall by release of inflammatory factors even though there is no distinct structural change on the arterial walls under light microscope, indicating that passive cigarette smoking is related to inflammatory injury in human arterial wall and could be closely related to the early inflammatory stage of atherosclerosis.
